The relationship between proved viral bronchiolitis and subsequent wheezing

doi:10.1016/S0022-3476(71)80385-2

The Journal of Pediatrics

Volume 79, Issue 5, November 1971, Pages 744-747

https://doi.org/10.1016/S0022-3476(71)80385-2 Get rights and content

Sixty-two children who had bronchiolitis in infancy associated with isolation of respiratory syncytial virus were reviewed at ages ranging from 2 to 7 years. Thrity-five (56 per cent) had had further wheezing, and 27 (43 per cent) had wheezed on more than 5 occasions. There was a significantly higher incidence of asthma in first degree relatives of those infants who developed recurrent wheezing in comparison with those of infants who did not.

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Cited by (165)

The Role of Antiviral Strategies for the Prevention of Childhood Asthma
2016, Allergy, Immunity and Tolerance in Early Childhood: The First Steps of the Atopic March
This chapter reviews antiviral treatments of interest to decrease the risk for childhood-onset asthma. Most antiviral options are aimed at treating the acute effects of virus infection that provoke wheezing or are prophylactic treatments administered to high-risk infants. Alternatively, antiviral vaccines would have the advantage of stimulating an adaptive immune response to modify the adverse effects of the same viral pathogen later on. However, effective vaccines for the respiratory syncytial virus and rhinovirus, the pathogens most often associated with wheezing, have been difficult to produce. Other environmental risk factors, in particular sensitization and exposure to environmental allergens, also influence the development of asthma. Thus, it may be necessary to combine specific antiviral treatments with methods to counter the adverse effects of allergic inflammation, and/or to normalize gut, skin, and airway microbiota to decrease the risk for future wheeze.
Natural helper cells contribute to pulmonary eosinophilia by producing IL-13 via IL-33/ST2 pathway in a murine model of respiratory syncytial virus infection
2015, International Immunopharmacology
Citation Excerpt :
Provirus studies indicated that infection with RSV induces Th2-like cytokine production as well as specific IgE antibody response, and then augments the risk for the development of allergic asthma [5–7]. RSV infection affects airway function through viral- and inflammation-induced damage [3,8,9]. It has been reported that airway infection with RSV causes bronchial hyperreactivity in association with an increase in eosinophils, that are recognized as proinflammatory granulocytes during parasitic infections and allergic diseases [10,11].
It has been reported that natural helper cells, which are a non-T, non-B innate lymphoid cell type expressing c-Kit and ST2, mediate influenza-induced airway hyper-reactivity by producing substantial IL-13. However, little is known about natural helper cells for the development of RSV-induced airway inflammation, particularly eosinophilic infiltration. By using BALB/c mice that were infected intranasally with RSV, it became clear that infection with RSV can induce an increase in the absolute number of natural helper cells in the lungs of mice. It seems likely that these natural helper cells contribute to the massive eosinophilic infiltration in an IL-13-dependent manner. In fact, the number of IL-13-producing natural helper cells as well as the expression of IL-13 mRNA in natural helper cells was enhanced significantly during RSV infection, suggesting that natural helper cells might be cellular source of the Th2-type cytokine IL-13. Indeed, adoptive transfer of pulmonary natural helper cells augmented not only the production of IL-13 but also the infiltration of eosinophils in the lungs of transferred mice. Pulmonary natural helper cells can produce IL-13 following response to IL-33, which was increased markedly in the lungs of mice after intranasal RSV infection. The expression of IL-13 mRNA in pulmonary natural helper cells was up-regulated by in vitro IL-33 stimulation. Furthermore, blockade of IL-33 receptor subunit, ST2, diminished the frequency of IL-13-producing natural helper cells. Taken together, these results demonstrate that natural helper cells may play an important role in RSV-induced pulmonary eosinophilia by producing IL-13 via the IL-33/ST2 pathway.
The Role of Antiviral Strategies for the Prevention of Childhood Asthma
2015, Allergy, Immunity and Tolerance in Early Childhood: The First Steps of the Atopic March
This chapter reviews antiviral treatments of interest to decrease the risk for childhood-onset asthma. Most antiviral options are aimed at treating the acute effects of virus infection that provoke wheezing or are prophylactic treatments administered to high-risk infants. Alternatively, antiviral vaccines would have the advantage of stimulating an adaptive immune response to modify the adverse effects of the same viral pathogen later on. However, effective vaccines for the respiratory syncytial virus and rhinovirus, the pathogens most often associated with wheezing, have been difficult to produce. Other environmental risk factors, in particular sensitization and exposure to environmental allergens, also influence the development of asthma. Thus, it may be necessary to combine specific antiviral treatments with methods to counter the adverse effects of allergic inflammation, and/or to normalize gut, skin, and airway microbiota to decrease the risk for future wheeze.
Elevated risk of asthma after hospitalization for respiratory syncytial virus infection in infancy
2013, Paediatric Respiratory Reviews
Citation Excerpt :
An additional four articles wherein wheezing was sufficiently severe to potentially indicate asthma,37–40 as well as one already reviewed for asthma that estimated recurrent wheezing among younger children,4 were included. Two additional estimates (one cumulative 38 and one current4) of asthma prevalence in the <5 years of age category and three cumulative 37,39,40 and two current estimates 37,40 in the 5 to 11 years category were included. Inclusion of the prevalence estimates from these additional studies did not change the results; and upper and lower limits of the calculated estimates remained the same (Figure 5).
Severe respiratory syncytial virus (RSV) infection in infancy is associated with substantial morbidity worldwide; whether it is a risk factor for childhood asthma is contentious. A systematic review of 28 articles was conducted, summarizing estimates of asthma risk after RSV hospitalization during infancy. Prevalence estimates of asthma, among those hospitalized for RSV in infancy, were from 8% to 63%, 10% to 92%, and 37%, at ages <5, 5 to 11, and ≥12 years, respectively. These rates were higher than those among non-hospitalized comparisons. The attributable risk of asthma due to RSV ranged from 13% to 22% and from 11% to 27% among children aged ≤5 and aged 5 to 11, respectively, and was 32% among children ≥ 12 years of age. Overall, 59% of asthma prevalence estimates from those previously hospitalized for RSV exceeded 20%, compared to only 6% of non-hospitalized comparison estimates. Despite variability in asthma prevalence estimates after RSV-related hospitalization, available data suggest a link between severe RSV infection in infancy and childhood asthma.
Responsiveness to respiratory syncytial virus in neonates is mediated through thymic stromal lymphopoietin and OX40 ligand
2012, Journal of Allergy and Clinical Immunology
Citation Excerpt :
The interplay between RSV infection and asthma, especially the development of asthma, is not entirely clear.30 Severe RSV infection and the need for hospitalization have been linked to asthma development,2-4 but it is unclear whether reinfection plays a similar role as it does in enhancing respiratory disease severity. To approach these issues in an experimental model, we examined the responses to reinfection in mice initially infected as neonates or at a later age and demonstrated dramatic differences.8
Recent studies revealed a critical role for thymic stromal lymphopoietin (TSLP) released from epithelial cells and OX40 ligand (OX40L) expressed on dendritic cells (DCs) in T_H2 priming and polarization.
We sought to determine the importance of the TSLP-OX40L axis in neonatal respiratory syncytial virus (RSV) infection.
Mice were initially infected with RSV as neonates or adults and reinfected 5 weeks later. Anti-OX40L or anti-TSLP were administered during primary or secondary infection. Outcomes included assessment of airway function and inflammation and expression of OX40L, TSLP, and IL-12.
OX40L was expressed mainly on CD11c⁺MHC class II (MHCII)⁺CD11b⁺ DCs but not CD103⁺ DCs. Treatment of neonates with OX40L antibody during primary RSV infection prevented the subsequent enhancement of airway hyperresponsiveness and the development of airway eosinophilia and mucus hyperproduction on reinfection. Administration of anti-TSLP before neonatal RSV infection reduced the accumulation of lung DCs, decreased OX40L expression on lung DCs, and attenuated the enhancement of airway responses after reinfection.
In mice initially infected as neonates, TSLP expression induced by RSV infection is an important upstream event that controls OX40L expression, lung DC migration, and T_H2 polarization, accounting for the enhanced response on reinfection.
The relationship between RSV bronchiolitis and recurrent wheeze: The chicken and the egg
2011, Early Human Development
Citation Excerpt :
The aim of this review is to provide a brief overview of our current understanding of the complex pathogenesis of RSV bronchiolitis and PBW. A number of retrospective studies since the 1970s have described a clear association between RSV bronchiolitis and increased risk for subsequent wheezing [4,5]. Because of the retrospective methodology of those initial studies, several authors raised questions about the significance of this association.
Respiratory syncytial virus bronchiolitis is the most frequent cause of infant hospitalization. RSV bronchiolitis is often followed by recurrent episodes of wheeze. Pathogenesis of RSV bronchiolitis as well as post-bronchiolitis wheeze are incompletely understood. The aim of this review is to provide a brief overview of our current understanding of the complex pathogenesis of RSV bronchiolitis and post-bronchiolitis wheeze. Two non-exclusive hypotheses exist, which are paraphrased for this review as “the chicken and the egg”. First, we reviewed the pre-existent genetic, pulmonary and immunological mechanisms of RSV bronchiolitis and post-bronchiolitis wheeze. Second, RSV as the causative virus of long-term airway morbidiy is reviewed. Clearly, RSV infection is capable of causing direct damage to the airways and/or inducing long-term inappropriate immune responses to respiratory viruses or aero-allergens. It is concluded that intervention trials aimed at preventing RSV infections are required to establish the relative contribution of both RSV-induced and pre-existent mechanisms to the development of long-term airway disease following RSV bronchiolitis.

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^*: Royal Children's Hospital Research Foundation, Melbourne, Australia.

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Original articleThe relationship between proved viral bronchiolitis and subsequent wheezing

J. Allergy

J. Pediatr.

The relationship between bronchiolitis and childhood asthma

J. Allergy

Relationship of acute bronchiolitis to bronchial asthma

Pediatrics

Acute bronchiolitis and the asthmatic child

J. Asthma Res.

Original article
The relationship between proved viral bronchiolitis and subsequent wheezing